Genomic organization and embryonic expression of the mouse fibroblast growth factor 9 gene

Colvin, Jennifer S.; Feldman, Benjamin; Nadeau, Joseph H.; Goldfarb, Mitchell; Ornitz, David M.

doi:10.1002/(sici)1097-0177(199909)216:1<72::aid-dvdy9>3.0.co;2-9

Cited by 196 publications

(95 citation statements)

References 71 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Epicardial FGF is one of the major signals regulating myocardial growth and coronary vessel formation during embryonic heart development. Both FGF-2 and FGF-9, and the FGF receptor FGFR1 are expressed in the heart during mouse development (Colvin et al, 1999). Since mice with a knockout for FGF-2 undergo normal heart development (Zhou et al, 1998;Schultz et al, 1999) whereas mice with a knockout for FGF-9 show reduced growth of the myocardium (Lavine et al, 2005), we examined epicardial FGF-9 signaling in B WT-1 /B WT-1 hearts.…”

Section: Nmiib Is Important For Epicardial Function To Support Myocarmentioning

confidence: 99%

Nonmuscle myosin IIB regulates epicardial integrity and epicardium-derived mesenchymal cell maturation

Sung

Yang

et al. 2017

Journal of Cell Science

View full text Add to dashboard Cite

Nonmuscle myosin IIB (NMIIB; heavy chain encoded by MYH10) is essential for cardiac myocyte cytokinesis. The role of NMIIB in other cardiac cells is not known. Here, we show that NMIIB is required in epicardial formation and functions to support myocardial proliferation and coronary vessel development. Ablation of NMIIB in epicardial cells results in disruption of epicardial integrity with a loss of E-cadherin at cell-cell junctions and a focal detachment of epicardial cells from the myocardium. NMIIB-knockout and blebbistatin-treated epicardial explants demonstrate impaired mesenchymal cell maturation during epicardial epithelial-mesenchymal transition. This is manifested by an impaired invasion of collagen gels by the epicardium-derived mesenchymal cells and the reorganization of the cytoskeletal structure. Although there is a marked decrease in the expression of mesenchymal genes, there is no change in Snail (also known as Snai1) or E-cadherin expression. Studies from epicardiumspecific NMIIB-knockout mice confirm the importance of NMIIB for epicardial integrity and epicardial functions in promoting cardiac myocyte proliferation and coronary vessel formation during heart development. Our findings provide a novel mechanism linking epicardial formation and epicardial function to the activity of the cytoplasmic motor protein NMIIB.

show abstract

Section: Nmiib Is Important For Epicardial Function To Support Myocarmentioning

confidence: 99%

Nonmuscle myosin IIB regulates epicardial integrity and epicardium-derived mesenchymal cell maturation

Sung

Yang

et al. 2017

Journal of Cell Science

View full text Add to dashboard Cite

show abstract

“…At the condensation stage, Fgf9 is expressed within condensing mesenchyme ( Fig. 3B; Colvin et al 1999). However, in the absence of FGF9 there are no apparent defects in skeletal development (Colvin et al 2001a,b).…”

Section: Fgf Signaling In Condensing Mesenchymementioning

confidence: 99%

“…However, no defects in chondrogenesis were observed (Montero et al 2000). Fgf9 is also expressed in chondrocytes (Colvin et al 1999;Garofalo et al 1999). However, the skeleton of Fgf9 −/− mice is apparently normal at birth when these mice die of other causes (Colvin et al 2001a,b).…”

Section: Expression Of Fgfs and Fgf Receptors In Endochondral Bonementioning

confidence: 99%

FGF signaling pathways in endochondral and intramembranous bone development and human genetic disease

Ornitz¹,

Marie²

2002

Genes Dev.

Self Cite

820

648

View full text Add to dashboard Cite

Over the last decade the identification of mutations in the receptors for fibroblast growth factors (FGFs) has defined essential roles for FGF signaling in both endochondral and intramembranous bone development. FGF signaling pathways are essential for the earliest stages of limb development and throughout skeletal development. In this review, we examine the role of FGF signaling in bone development and in human genetic diseases that affect bone development. We also explore what is presently known about how FGF signaling pathways interact with other major signaling pathways that regulate chondrogenesis and osteogenesis.

show abstract

“…There are 22 Fgf genes in humans and mice, several of which are expressed in partially overlapping and dynamic patterns in the developing mouse facial primordia (FrancisWest et al, 1998;Colvin et al, 1999;Bachler and Neubuser, 2001). In particular, Fgf8 is expressed broadly in the frontonasal and mandibular epithelia before outgrowth of the nasal processes and its expression becomes highly localized to around the nasal pits as well as in the maxillary and mandibular epithelia during active facial primordial outgrowth (Bachler and Neubuser, 2001; Fig.…”

Section: The Fgf Pathwaymentioning

confidence: 99%

Development of the upper lip: Morphogenetic and molecular mechanisms

Jiang

Bush

Lidral

2005

Developmental Dynamics

288

304

View full text Add to dashboard Cite

The vertebrate upper lip forms from initially freely projecting maxillary, medial nasal, and lateral nasal prominences at the rostral and lateral boundaries of the primitive oral cavity. These facial prominences arise during early embryogenesis from ventrally migrating neural crest cells in combination with the head ectoderm and mesoderm and undergo directed growth and expansion around the nasal pits to actively fuse with each other. Initial fusion is between lateral and medial nasal processes and is followed by fusion between maxillary and medial nasal processes. Fusion between these prominences involves active epithelial filopodial and adhering interactions as well as programmed cell death. Slight defects in growth and patterning of the facial mesenchyme or epithelial fusion result in cleft lip with or without cleft palate, the most common and disfiguring craniofacial birth defect. Recent studies of craniofacial development in animal models have identified components of several major signaling pathways, including Bmp, Fgf, Shh, and Wnt signaling, that are critical for proper midfacial morphogenesis and/or lip fusion. There is also accumulating evidence that these signaling pathways cross-regulate genetically as well as crosstalk intracellularly to control cell proliferation and tissue patterning. This review will summarize the current understanding of the basic morphogenetic processes and molecular mechanisms underlying upper lip development and discuss the complex interactions of the various signaling pathways and challenges for understanding cleft lip pathogenesis.

show abstract

Genomic organization and embryonic expression of the mouse fibroblast growth factor 9 gene

Cited by 196 publications

References 71 publications

Nonmuscle myosin IIB regulates epicardial integrity and epicardium-derived mesenchymal cell maturation

Nonmuscle myosin IIB regulates epicardial integrity and epicardium-derived mesenchymal cell maturation

FGF signaling pathways in endochondral and intramembranous bone development and human genetic disease

Development of the upper lip: Morphogenetic and molecular mechanisms

Contact Info

Product

Resources

About